Posttraumatic stress disorder is associated with enhanced interleukin-6 response to mental stress in subjects with a recent myocardial infarction

• Published in: Brain, behavior, and immunity Vol. 75; pp. 26 - 33
• Main Authors: Lima, Bruno B., Hammadah, Muhammad, Wilmot, Kobina, Pearce, Brad D., Shah, Amit, Levantsevych, Oleksiy, Kaseer, Belal, Obideen, Malik, Gafeer, Mohamad Mazen, Kim, Jeong Hwan, Sullivan, Samaah, Lewis, Tené T., Weng, Lei, Elon, Lisa, Li, Lian, Bremner, J. Douglas, Raggi, Paolo, Quyyumi, Arshed, Vaccarino, Viola
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.01.2019
• Subjects: Adult; Biomarkers; C-Reactive Protein - analysis; Chemokine CCL2 - analysis; Chemokine CCL2 - blood; Female; High-sensitivity C reactive protein; Humans; Inflammation - complications; Intercellular Adhesion Molecule-1; Interleukin-6; Interleukin-6 - metabolism; Male; Matrix metallopeptidase 9; Mental stress; Middle Aged; Monocyte chemoattractant protein-1; Myocardial infarction; Myocardial Infarction - complications; Myocardial Infarction - psychology; PTSD; Stress Disorders, Post-Traumatic - complications; Stress Disorders, Post-Traumatic - immunology; Stress Disorders, Post-Traumatic - metabolism; Stress, Psychological - immunology; Stress, Psychological - metabolism; Vascular Cell Adhesion Molecule-1; Myocardial infarction; Monocyte chemoattractant protein-1; MCP-1; ICAM-1; Matrix metallopeptidase 9; IL-6; Interleukin-6; PTSD; VCAM-1; High-sensitivity C reactive protein; MI; HsCRP; MMP-9; Mental stress
• ISSN: 0889-1591; 1090-2139; 1090-2139
• DOI: 10.1016/j.bbi.2018.08.015

•MI patients with PTSD show enhanced IL-6 response to stress than those without PTSD.•This effect is mainly driven by the re-experiencing symptom cluster of PTSD.•Our data suggest a mechanistic link between PTSD and poor cardiovascular outcomes. Posttraumatic Stress Disorder (PTSD) is prevalent among patients who survived an acute coronary syndrome, and is associated with adverse outcomes, but the mechanisms underlying these associations are unclear. Individuals with PTSD have enhanced sensitivity of the noradrenergic system to stress which may lead to immune activation. We hypothesized that survivors of a myocardial infarction (MI) who have PTSD would show an enhanced inflammatory response to acute psychological stress compared to those without PTSD. Individuals with a verified history of MI within 8 months and a clinical diagnosis of current PTSD underwent a mental stress speech task. Inflammatory biomarkers including interleukin-6 (IL-6), high-sensitivity C reactive protein (HsCRP), matrix metallopeptidase 9 (MMP-9), intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and monocyte chemoattractant protein (MCP)-1 were measured at rest and 90 min after mental stress. Among 271 patients in the study (mean age 51 ± 7 years, 50% female, 60% African-American), the prevalence of PTSD was 12%. Mental stress resulted in a significant increase in IL-6, but the increase was more marked in patients with PTSD (126% increase) than those without (63% increase) (p = 0.001). MCP-1 showed a modest increase with stress which was similar in patients with PTSD (9% increase) and without PTSD (6% increase) (p = 0.35). CRP did not increase with stress in either group. MI patients with current PTSD exhibit enhanced IL-6 response to psychosocial stress, suggesting a mechanistic link between PTSD and adverse cardiovascular outcomes as well as other diseases associated with inflammation.